Previous studies have implicated the cerebellum as having a role in both seizure production and its prevention by anticonvulsants. That altered cerebral energy metabolism is involved in the seizure state has been known for a long time, but recent evidence based on single cell analysis indicates that Purkinje cells may be spared this alteration, even in the presence of maximal electroshock. Such a sparing effect on Purkinje cell output may be permissive to the seizure state. It is important in future studies to examine effects in single cells since inclusion of contiguous tissue may dilute the sample masking more pronounced changes. In this proposed study, we intend to directly assess energy metabolism, GABA levels, and turnover, in single neurons. These studies will be done in small mice in which seizures have been induced by electroshock, isoniazid treatment, or audiogenic stimulation. Some animals will be pretreated with phenytoin, sodium valproate, or clonazepam. Following sacrifice in liquid N2, the brains will be processed for metabolite analysis. The energy metabolites ATP, P-creatine, glucose, and glycogen, as well as GABA will be measured in cortical pyramidal cells, cerebellar Purkingje cells, and adjacent neuropil. Results from these studies should provide new direct evidence as to the mechanisms involved in the seizure state and its prevention with anticonvulsants.